Cardiovascular Mechanisms of Longitudinal Performance Decline in Master Athletes:

A Revisão NarrativaA narrative review is a type of scientific article that synthesizes existing research on a topic through expert selection and interpretation rather than through a pre-registered, exhaustive search with formal bias scoring; unlike a systematic review or meta-analysis, its conclusions can reflect the authors' editorial judgment in choosing which studies to emphasize. of Aging, Coronary Artery DiseaseA doença arterial coronariana é o acúmulo de placas nas artérias que irrigam o músculo cardíaco., Silent Myocardial IsquemiaIsquemia é quando um tecido não está recebendo sangue e oxigênio suficientes para o que lhe está sendo exigido., and Unrecognized Infarto do miocárdioVeja Ataque Cardíaco para o verbete completo.

Resumo

This narrative review synthesizes selected peer-reviewed evidence on the cardiovascular and physiological mechanisms underlying longitudinal performance decline in master athletes between the ages of 50 and 80. Topics addressed include (1) the natural trajectory of physical capacity from the Swedish Population Cohort for Physical Activity and Fitness (SPAF) study[1]; (2) the contrast between master-athlete and sedentary V̇O₂max decline[2][3][4]; (3) central and peripheral cardiovascular mechanisms of V̇O₂max erosion; (4) the paradox of subclinical coronary ateroscleroseA aterosclerose é a doença por trás da maioria dos ataques cardíacos e de muitos acidentes vasculares cerebrais. Partículas de colesterol ficam presas na parede de uma artéria, o corpo envia células imunológicas para limpar e, ao longo dos anos, essa bagunça endurece, transformando-se em placa. in lifelong endurance athletes; (5) silent myocardial ischemia and unrecognized myocardial infarction — including epidemiologiaA epidemiologia é o estudo dos padrões de saúde em grandes grupos de pessoas — quem adoece, onde e o que eles tinham em comum., mechanisms, prognosis, and diagnostic approach; (6) coronary disfunção microvascularMicrovascular dysfunction is disease in the smallest blood vessels of the heart, too small to see on any angiogram. as a candidate contributor to exercise intolerance in selected older athletes; and (7) contemporary sports-cardiology screening considerations grounded in the Diretriz da ESC de 2020 sobre Cardiologia do EsporteThe 2020 ESC Sports Cardiology Guideline is the European Society of Cardiology's evidence-based document providing recommendations on cardiovascular screening, risk stratification, and return-to-sport decisions for competitive and recreational athletes, including master athletes with suspected or established heart disease.. The synthesis is interpretive rather than exhaustive; specific search strategy and scope are described in the Literature Identification section.

1. Introdução

The aging process in humans is inexorably linked to a progressive decline in physiological capacity, yet the rate and trajectory of this decline are significantly influenced by habitual physical activity. Among individuals who maintain high levels of endurance training into their sixth, seventh, and eighth decades — commonly referred to as master athletes — the decline in maximal aerobic capacity (V̇O₂max) and endurance performance provides a unique biological model for studying the limits of human aging[2]. While master athletes consistently demonstrate superior aptidão cardiorrespiratóriaCardiorespiratory fitness is how well your heart, lungs, and muscles work together to use oxygen during hard exercise. It is often measured as VO2 max. (CRF) compared to their sedentary peers, they are not immune to the fundamental biological processes that erode cardiovascular function over time[3][4].

Longitudinal performance decline between the ages of 50 and 80 is governed by a complex interplay of central cardiac limitations, peripheral vascular and mitochondrial decay, and the paradoxical emergence of subclinical cardiovascular pathologies. These include coronary artériaUma artéria é um vaso sanguíneo que transporta o sangue do coração para o resto do corpo. disease in lifelong endurance athletes[13][14][15] and, in the broader aging population, silent myocardial ischemia (SMI)Silent myocardial ischemia is reduced blood flow to the heart during exertion that produces no chest pain or recognizable symptoms; in master athletes, elevated pain thresholds from years of training can mask this warning sign entirely., unrecognized myocardial infarction (UMI)An unrecognized myocardial infarction is a heart attack that occurred without being identified at the time, leaving a permanent scar on the heart muscle that is only discovered later through imaging or electrocardiography., e coronary microvascular dysfunction (CMD)Coronary microvascular dysfunction is impaired function of the tiny arterioles and capillaries supplying the heart muscle, resulting in reduced blood flow and exercise intolerance even when the major coronary arteries appear normal on angiography.[21][22]. To understand these mechanisms in context, it is helpful first to establish a population-level baseline from the SPAF longitudinal cohort[1] and then to contrast that baseline with the specific physiological adaptations — and pathological risks — observed in lifelong endurance athletes.

2. Literature Identification

This article is a narrative review. Literature was identified primarily through PubMed and Embase searches (1990–2026) and by backward reference review of relevant primary studies, meta-analyses, and major-society guidance documents addressing master athletes, age-related decline in aerobic capacity, coronary atherosclerosis in endurance athletes, silent myocardial ischemia, unrecognized myocardial infarction, coronary microvascular dysfunction, and sports-cardiology screening. Priority was given to original cohort studies, randomized trials, systematic reviewsA systematic review searches for every study on a question using a pre-declared method, then assesses them by consistent criteria., meta-analyses, and official guideline statements. Because this was not a protocol-driven systematic review, study selection was qualitative and the synthesis should be interpreted as interpretive rather than exhaustive. No formal meta-analytic pooling was performed; quantitative values are reproduced from the cited primary sources without re-analysis.

3. The General Population Baseline: Insights from the Westerståhl SPAF Study

The 47-year longitudinal SPAF study reported by Westerståhl and colleagues offers one of the most comprehensive assessments of how physical capacity changes from adolescence into early old age in a representative general-population cohort[1]. Tracking 427 individuals born in 1958, the study used repeated objective assessments of aerobic capacity, muscular endurance, and explosive power from age 16 to age 63[1]. The dataset is informative because it identifies the natural rate of decline in a population where physical activity is not standardized, highlighting the accelerating nature of biological aging regardless of elite athletic status.

Peak physical performance was generally attained between the ages of 26 and 36 for both absolute aerobic capacity and muscular endurance[1]. Specifically, men reached their peak absolute aerobic capacity at age 35 (3.26 L·min⁻¹), while women peaked at age 36 (2.61 L·min⁻¹)[1]. After these peaks, decline began at approximately 0.3–0.6% per year and accelerated to roughly 2.0–2.5% per year as participants approached their 60s[1]. By age 63, cumulative decline in absolute aerobic capacity from peak was approximately 33% in men and 30% in women[1].

Tabela 1. Physical capacity trajectories from the 47-year SPAF longitudinal cohort.

Parâmetro	Men (peak age 35–36)	Women (peak age 36)	Total decline by 63
Absolute aerobic capacity (L·min⁻¹)	3.26	2.61	30–33%
Relative aerobic capacity (mL·kg⁻¹·min⁻¹)	42.2 at age 26	39.7 at age 31	37–40%
Vertical jump (cm)	45.5 at age 27	33.0 at age 19	41–48%
Muscular endurance (bench press, reps)	52.7 at age 36	39.7 at age 34	32–35%

Source: Westerståhl M, et al. J Cachexia SarcopeniaA sarcopenia é a perda progressiva de massa e força muscular que acompanha a idade. Muscle. 2025[1]. Values are cohort means at the indicated age. SPAF = Swedish Population Cohort for Physical Activity and Fitness.

The SPAF data also underscored the role of lifestyle factors in modifying these trajectories. Higher leisure-time physical activity at age 16 and an active lifestyle during adulthood were associated with superior performance across all metrics throughout life[1]. Higher educational attainment was associated with higher absolute aerobic capacity and muscular endurance, plausibly via health-seeking behaviors. Even with these protective factors, however, the acceleration of decline after age 40 was a consistent finding, reinforcing the concept that biological aging imposes a progressive physiological constraint on functional capacity that begins to operate well before it becomes clinically significant.

4. Comparative Decline: Master Athletes vs. General Population

When contrasting the SPAF baseline with longitudinal data from master athletes, a clear distinction emerges in starting altitude and slope of V̇O₂max decline. Master endurance athletes represent a cohort that has maximized adaptive potential and may carry a V̇O₂max at age 60 that exceeds the median for a sedentary 40-year-old[2]. Despite this advantage, the inevitable decline in V̇O₂max remains the primary physiological mechanism associated with reduced endurance performance in aging athletes[3][4].

Longitudinal assessments indicate that master athletes who maintain high-intensity, high-volume training reduce the rate of V̇O₂max decline to approximately 5–7% per decade, compared with 10–12% per decade in age-matched sedentary individuals[2][3][4]. This training-attenuated decline is, however, fragile; regression analyses indicate that a substantial proportion of the variance in V̇O₂max decline in master athletes is directly attributable to reductions in training volume and intensity, with steepest declines (15–46% per decade) observed in athletes who substantially reduce training[3][4].

Tabela 2. Decadal rates of V̇O₂max decline by group.

Group	Decadal decline	Primary driver
Sedentary adults	10–12%	Sarcopenia, inactivity, central cardiac decline
Master athletes (maintained training)	5–7%	Intrinsic decline in maximal frequência cardíacaA frequência cardíaca é o número de vezes que o seu coração bate por minuto.
Master athletes (reduced training)	15–46%	Detraining superimposed on aging

Sources: refs [2][3][4].

5. Cardiovascular Mechanisms of Aerobic Capacity Erosion

The erosion of V̇O₂max is mathematically described by the Fick principleThe Fick principle states that maximal oxygen consumption equals cardiac output multiplied by the arteriovenous oxygen content difference; it provides the mathematical framework for separating how much of an athlete's aerobic decline is due to a weakening heart pump versus reduced oxygen extraction by the muscles.: V̇O₂max = Q̇ × (a–v)O₂ difference, where Q̇ is cardiac output and (a–v)O₂ is the arteriovenous oxygen content difference. In master athletes, the relative contribution of central cardiac factors (heart rate and volume sistólicoO volume sistólico é a quantidade de sangue que o coração bombeia a cada batimento; em atletas masters, o treinamento crônico promove ventrículos maiores e mais complacentes que mantêm volumes sistólicos mais elevados, compensando parcialmente a inevitável queda da frequência cardíaca máxima relacionada à idade.) versus peripheral factors (oxygen extraction) shifts with age[8][9].

5.1 Central mechanisms: the aging pump

The most consistent and largely unmodifiable driver of V̇O₂max decline is the age-related reduction in maximal heart rate (HR_max). The widely cited Tanaka equationThe Tanaka equation estimates maximum heart rate as 208 minus 0.7 times a person's age; it predicts that maximum heart rate falls by roughly one beat per minute every year regardless of training status. — HR_max ≈ 208 − 0.7 × age — implies an average decline of approximately 0.7 beats·min⁻¹ per year[7]. This is driven primarily by changes in the intrinsic electrophysiology of the sinoatrial nodeThe sinoatrial node is a small cluster of specialized cells in the right atrium that generates the electrical impulse triggering each heartbeat; it acts as the heart's natural pacemaker, and its intrinsic firing rate declines with age independently of fitness level. and by reduced β-adrenergic responsivenessβ-adrenergic responsiveness refers to the heart's sensitivity to stimulation by adrenaline and related stress hormones via beta-adrenergic receptors; aging reduces this sensitivity, limiting how fast and forcefully the heart can respond during peak exercise even in highly trained individuals. with age. While endurance training can lower resting heart rate and enhance parasympathetic tone, it has limited ability to preserve maximal heart rate during all-out exertion.

Acidente vascular cerebralUm AVC ocorre quando o fluxo sanguíneo para uma parte do cérebro é interrompido, seja por um bloqueio ou por sangramento. volume (SV) provides a more nuanced story. In sedentary individuals, SV declines due to increased myocardial stiffness, reduced ventricular compliance, and impaired diastolic filling[10]. In master athletes, chronic endurance training induces eccentric ventricular remodeling characterized by larger chamber dimensions and enhanced myocardial compliance[10][11]. This adaptation allows athletes to maintain higher SV through the Frank-Starling mechanismThe Frank-Starling mechanism is the heart's intrinsic ability to increase the force of contraction when more blood fills the ventricle during diastole; master athletes exploit this by developing larger, more compliant ventricles that can pump greater stroke volumes even as maximum heart rate falls.. Nonetheless, master athletes can experience reduced SV at peak exercise due to abnormal shortening of diastolic filling time at very high heart rates, where the diastolic interval is too short for complete ventricular filling.

5.2 Peripheral mechanisms: oxygen extraction and mitochondrial decay

While central limitations dominate the early phases of decline, peripheral factors become increasingly limiting as athletes approach age 80[9]. Three peripheral processes are most consequential:

• Arteriovenous O₂ Maximal (a–v)O₂ difference declines modestly with age in master athletes, largely driven by capillary rarefactionCapillary rarefaction is the age-related loss of capillary density within skeletal muscle, which increases the distance oxygen must travel from blood to muscle fibers and reduces the efficiency of oxygen extraction during exercise. — thinning of the capillary networks supplying individual muscle fibrasA fibra é a parte do alimento vegetal que seu corpo não consegue digerir. Ela é encontrada em feijões, aveia, vegetais, frutas e grãos integrais. — which increases diffusion distance for oxygen[9].
• Mitochondrial function. Aging is associated with reductions in mitochondrial densityThe concentration of mitochondria within muscle fibers, which determines the cell's capacity for aerobic energy production; endurance training is associated with preserving mitochondrial density in older athletes. and in the activity of key oxidative enzymes such as citrate synthase and succinate dehydrogenase[2]. Maintenance of high-intensity training in master athletes preserves mitochondrial quality, but reductions in training volume produce a rapid, near-linear drop in oxidative capacity.
• Selective atrophy of Type II (fast-twitch) fibers and overall muscle-mass loss reduces metabolic demand and exercise output, an effect documented in the SPAF cohort and elsewhere[1].

6. Coronary Atherosclerosis in Master Athletes: The Calcification Paradox

One of the most challenging findings in modern sports cardiology is the apparent paradox of high escore de cálcio coronariano (ECC)O cálcio arterial coronariano é uma medida dos depósitos de placa calcificada nas paredes das artérias coronárias, quantificada por tomografia computadorizada e expressa como um escore de Agatston; escores mais altos indicam maior carga cumulativa de placa e predizem futuros eventos cardiovasculares. scores in lifelong endurance athletes. Cross-sectional data, including the Master@Heart cohort, have shown that lifelong endurance athletes (predominantly male) often carry a higher prevalence of coronary placasPlaca é o acúmulo de colesterol, células imunológicas, tecido cicatricial e cálcio dentro da parede de uma artéria. and higher CAC scores than sedentary peers of similar risk profile[13][14][15][16][17].

6.1 Plaque morphology and distribution

O Estudo Master@HeartThe Master@Heart study is a controlled study of lifelong male endurance athletes that found they carried more total coronary plaque than healthy, active non-athletes—including more calcified and non-calcified plaque in proximal artery segments—raising questions about whether extreme lifelong endurance training promotes atherosclerosis even in the absence of traditional risk factors. by De Bosscher and colleagues enrolled 191 lifelong athletes, 191 late-onset athletes, and 176 healthy non-athletes (all male) and demonstrated that lifelong athletes had the highest coronary carga de placaPlaque burden is the total amount of plaque in your arteries, everywhere — not just at the single worst spot.[15]. The burden included not only placas calcificadasCalcified plaque is the hardened, calcium-filled part of a plaque. It shows up brightly on a CT scan, which is what a calcium scan measures. — generally considered stable — but also non-calcified and mixed plaques in proximal coronary segmentsThe proximal coronary segment refers to the portion of a coronary artery closest to its origin from the aorta; plaques in these segments are considered highest risk because blockages there can cut off blood supply to the largest area of heart muscle.[15].

Tabela 3. Coronary plaque findings from the Master@Heart cohort.

Group	≥1 coronary plaque (OR)	≥1 proximal plaque (OR)	≥50% luminal estenoseStenosis is narrowing — usually described as a percentage, like a 70 percent blockage.
Non-athletes (reference)	1.00	1.00	≈ reference
Late-onset athletes	intermediate	intermediate	low
Lifelong endurance athletes	1.86	1.96	uncommon, but elevated vs. controls

Source: De Bosscher R, et al. Eur Heart J. 2023[15]. OR = odds ratio versus non-athlete reference; values are adjusted estimates. All participants were male; mean age ≈ 60 years. Obstructive (≥50%) stenosis was uncommon in absolute terms across all groups; exact reported prevalence in the lifelong-athlete arm should be cross-checked against the primary publication before final typesetting.

In Master@Heart, lifelong athletes were also disproportionately likely to have non-calcified plaquesNon-calcified plaque is the soft, fatty portion of a plaque that has not hardened with calcium. It shows up dark on a CT scan. in proximal segments compared with non-athletes[15]. Proximal location is clinically relevant because such plaques control flow to large myocardial territories. While higher cardiorespiratory fitness is associated with stable plaque morphology in some analyses, the absolute presence of these lesõesNa cardiologia, uma lesão refere-se a uma área delimitada de placa aterosclerótica que estreita uma artéria coronária, normalmente descrita pela porcentagem de obstrução luminal que causa. O artigo descreve quatro lesões residuais cujo diâmetro do vaso é pequeno demais para permitir a implantação de um stent após o tratamento da lesão mais crítica. suggests that high-volume endurance training may interact with conventional fatores de riscoUm fator de risco é algo que aumenta a sua chance de desenvolver uma doença — partículas de colesterol alto, pressão alta, tabagismo, diabetes, histórico familiar. to accelerate progression of pre-existing subclinical disease[16][17].

6.2 Proposed mechanistic drivers

The development of CAD in master athletes remains incompletely explained. The current observational literature raises several proposed mechanisms, which should be interpreted as plausible hypotheses rather than established causal pathways:

• Hemodynamic shear stress. Vigorous exercise produces hyperdynamic coronary flow. At sites of disturbed or turbulent flow, mechanical forces may contribute to disfunção endotelialEndothelial dysfunction is when that thin lining stops doing its job well. Vessels don't widen properly, and the barrier gets leakier.[13][17].
• Oxidative stressOxidative stress is an imbalance between damaging reactive molecules and the body's ability to neutralize them.. Extreme metabolic demands of ultra-endurance training may transiently generate espécies reativas de oxigênioReactive oxygen species are unstable oxygen-containing molecules produced as a by-product of normal metabolism. in excess of antioxidanteUm antioxidante é uma substância que elimina moléculas nocivas no corpo. A vitamina E e o betacaroteno são exemplos. capacity, with possible downstream effects on função endotelialA capacidade do revestimento interno dos vasos sanguíneos de regular o tônus vascular, a inflamação e a coagulação; células endoteliais saudáveis liberam óxido nítrico para manter as artérias relaxadas e resistentes à formação de placas. e lipoproteínaUma lipoproteína é um pequeno pacote que transporta gordura e colesterol através da sua corrente sanguínea. Como a gordura não se dissolve em água, ela precisa de um invólucro de proteína para viajar. retention[17].
• Exercise-induced hipertensãoHipertenção é o termo médico para pressão arterial alta.. In a recent cohort of male master endurance athletes, occult resting and exercise-induced hypertension was prevalent and associated with higher coronary plaque burden[18]. Exaggerated exercise pressão arterial sistólicaSystolic blood pressure is the top number — the pressure in your arteries while your heart is squeezing. responses are increasingly recognized as a clinically actionable phenotype.
• Interactions with conventional risk factors. Even in athletes, conventional risk factors — LDL-cholesterol, apolipoproteínaUma apolipoproteina é uma proteína ligada a uma partícula transportadora de gordura no sangue. A gordura e a água não se misturam, portanto, essas proteínas agem como um invólucro que permite que a gordura viaje com segurança pela corrente sanguínea. B, lipoproteína(a)Lipoproteína(a), escrita como Lp(a) e pronunciada como "L-P-minúsculo-a", é uma partícula semelhante ao LDL com uma proteína extra pegajosa anexada., hypertension, histórico familiarFamily history means whether your close relatives developed heart disease, and how young they were when it happened. — remain the dominant drivers of atherosclerosis[49][50].

7. Silent Myocardial Ischemia and Unrecognized Myocardial Infarction

7.1 Definitions and key distinction

Silent myocardial ischemia (SMI) refers to objective evidence of transient inducible ischemia — typically ST-segment depression on ambulatory or exercise ECG, or inducible perfusion abnormality on stress imaging — in the complete absence of anginal symptoms[21][22]. Unrecognized myocardial infarction (UMI) refers to a completed infarction that was not clinically diagnosed at the time it occurred[28][29][30][31]. Late gadolinium enhancementLate gadolinium enhancement (LGE) is a cardiac MRI technique in which a contrast agent accumulates in areas of scarred or fibrotic myocardium and appears bright on delayed imaging, indicating previous microscopic or clinical cardiac injury; 12–14% of masters athletes in the studies described showed this pattern, sometimes without any prior diagnosed heart attack. (LGE) on ressonância magnética cardíaca (RMC)A specialized MRI technique for the heart that can characterize the location, pattern, and extent of myocardial injury, helping distinguish ischemic infarction from non-ischemic conditions such as myocarditis or takotsubo syndrome. characterizes prior myocardial injury — scar, fibrosis, or completed infarction — and is therefore the reference standard imaging modality for UMI rather than a primary test for active ischemia[30][36]. This distinction is preserved throughout the remainder of this section.

7.2 Epidemiology of silent ischemia and unrecognized MI

Silent or unrecognized MIs account for a substantial fraction of all myocardial infarctions in epidemiological cohorts. The original Framingham Heart StudyThe Framingham Heart Study began in 1948 in one Massachusetts town and has now followed three generations of families. reported that approximately one-quarter of MIs were unrecognized when first detected during routine biennial examination[28]. The Atherosclerosis Risk in Communities (ARICARIC, o estudo Atherosclerosis Risk in Communities (Risco de Aterosclerose em Comunidades), tem acompanhado milhares de adultos americanos desde o final da década de 1980.) study found that the proportion of MIs that were silent and detected only by ECG was approximately 22%, with substantial sex and race differences in detection[29]. In the Cardiovascular Health Study of older community-dwelling adults, the prevalence of UMI rose with age[31].

The advent of cardiac MRICardiac MRI uses magnetic fields rather than X-rays to image the heart in fine detail, with no radiation. with LGE has substantially raised estimates of UMI prevalence. The ICELAND-MI study by Schelbert and colleagues found that UMI detected by CMR-LGE was more than twice as common as UMI detected by ECG in an older community cohort, and that ECG-detected UMI represented only a fraction of all CMR-detected events[30]. No MESAMESA, the Multi-Ethnic Study of Atherosclerosis, followed thousands of adults with no known heart disease, scanning their arteries and tracking outcomes. cohort, CMR-detected myocardial scar was identified in approximately 7.9% of asymptomatic adults aged 45–84 with no clinical history of MI[33].

Translated to US epidemiology, of the approximately 805,000 myocardial infarctions occurring annually in the United States, ECG-based community surveillance suggests that roughly 170,000 (≈21%) are clinically silent or unrecognized at the time of occurrence — a figure consistent with ARIC and Framingham proportions[28][29][31]. Because CMR-based detection has identified more than twice as many UMIs as ECG in older community cohorts[30], the ECG-based extrapolation of 170,000 is best interpreted as a lower bound on the true annual burden of clinically unrecognized myocardial infarction in the United States.

7.3 Why some myocardial ischemia and infarction is silent: proposed mechanisms

The absence of pain during ischemia or infarction is multifactorial. Eight broad mechanisms have been proposed in the literature:

• Autonomic neuropathy. Afferent sympathetic and vagal fibers that transmit cardiac nociceptive signals can be damaged by diabetesO diabetes é uma condição em que o açúcar no sangue permanece muito alto, seja porque o corpo produz pouca insulina ou porque para de responder à insulina que produz. mellitus, age-related autonomic neuropathy, or prior cardiac surgery, attenuating or eliminating the perception of ischemic pain[21].
• Higher pain threshold. Individuals vary substantially in baseline somatic pain thresholds, and a subset of patients with documented ischemia have demonstrably elevated thresholds for laboratory pain stimuli[34].
• Endogenous opioid and endocannabinoid systemsThe endocannabinoid system is a network of endogenous lipid signaling molecules and their receptors (including cannabinoid receptors CB1 and CB2) that modulates pain, mood, and energy balance throughout the nervous system. Research now indicates it plays a central role in exercise-induced hypoalgesia, with the runner's high depending on cannabinoid receptor signaling rather than opioid receptors…. Circulating β-endorphin and related opioids are elevated in some patients with isquemia silenciosaSilent ischemia is when the heart muscle is starved of oxygen but the person feels nothing at all. and have been implicated in central modulation of cardiac pain perception[34].
• Exercise-induced hypoalgesiaExercise-induced hypoalgesia is the reduction in pain perception that occurs during and after intense physical activity, caused by the release of endogenous opioids and other pain-dampening chemicals; in athletes, this effect can mask cardiac ischemia by blunting the chest pain that would otherwise signal inadequate blood flow to the heart. (EIH). Regular endurance training engages the endogenous opioid and endocannabinoid systems and is consistently associated with elevated pain thresholds and tolerances in laboratory testing[25][26]. In master athletes, EIH plausibly contributes to the absence of warning symptoms during demand-induced ischemia.
• Small infarct size and limited transmural extent. Small subendocardial or non-transmural infarcts may not generate sufficient afferent signaling to cross the threshold for conscious perception[32].
• Anatomic distribution. Inferior-wall ischemia and posterior-wall ischemia are more frequently silent than anterior-wall events, possibly due to differences in afferent innervation density[21].
• Collateral circulationA circulação colateral é uma rede de pequenos vasos sanguíneos de reserva que podem se desenvolver ao redor de uma artéria bloqueada, como um desvio em torno de uma estrada fechada.. Chronic exercise promotes the development of coronary collateral vessels, which can maintain blood flow distal to a stenosis at rest and during low-to-moderate exertion, thereby preventing ischemia and pain until peak demand exceeds collateral capacity[27].
• Ischemic preconditioningIschemic preconditioning is a protective cellular response in which a brief, sublethal episode of myocardial ischemia renders the heart more resistant to injury from a subsequent, more prolonged ischemic episode, mediated partly through mitochondrial K-ATP channels and adenosine release. It is one mechanism explaining why warm-up angina can disappear as exercise continues.. Repeated brief episodes of subclinical ischemia may protect the miocárdioThe myocardium is the muscular wall of the heart — the part that actually squeezes to push blood around your body. against subsequent insults and may also blunt afferent pain signaling[35].

7.4 Symptoms — and the absence of symptoms

By definition, classic exertional anginaAngina is chest discomfort that happens when the heart muscle isn't getting enough oxygen. People describe it as pressure, tightness, squeezing, or burning, and it can spread to the arm, neck, or jaw. is absent in silent ischemia and unrecognized MI. However, the term silent is sometimes a misnomer. On careful retrospective questioning, a proportion of patients with apparently silent events describe subtle symptoms at the time — most commonly unaccustomed dyspnea, exertional fatigue out of proportion to workload, atypical chest discomfort attributed to indigestion or musculoskeletal causes, syncope or near-syncope, or unexplained reduction in exercise tolerance[21][22][32]. These so-called anginal equivalents are particularly important in master athletes, in whom dropping performance — rather than chest pain — may be the only clinical warning. When no symptoms are reported in any form, the event is genuinely asymptomatic and is detected only through screening, incidental imaging, or as part of a subsequent workup.

7.5 Prognosis

Silent ischemia and unrecognized MI are not benign. In long-term follow-up of the ICELAND-MI cohort, UMI detected by CMR was associated with mortality comparable to that of clinically recognized MI[30]. Across multiple cohorts, individuals with UMI carry elevated risks of insuficiência cardíacaHeart failure means the heart cannot pump well enough to meet the body's needs. The name is misleading — it does not mean the heart has stopped., recurrent MI, and morte súbita cardíacaSudden cardiac death is when the heart abruptly stops and the person dies within minutes, often with no prior warning.[29][30][31]. In endurance athletes specifically, the presence of ischemic-pattern LGE has been associated with markedly elevated risk of subsequent major adverse eventos cardíacosClinically significant heart-related occurrences—including myocardial infarction, unstable angina, and cardiac death—used as outcome endpoints in cardiovascular trials. including sudden cardiac death[36].

7.6 Diagnosis

Diagnostic approaches differ for SMI versus UMI:

• For silent ischemia, the foundational modalities are ambulatory (Holter) ECG, exercise ECG, and stress imaging (stress echocardiography, single-photon emission CT, tomografia por emissão de pósitronsPositron emission tomography, or PET, uses a mildly radioactive tracer to show which tissues are metabolically busy., or stress CMR perfusion)[21][22].
• For unrecognized MI, the resting ECG de 12 derivaçõesUm eletrocardiograma padrão que registra a atividade elétrica do coração simultaneamente a partir de doze posições de eletrodos colocadas nos membros e no tórax; quando realizado durante o exercício máximo, pode revelar alterações isquêmicas — como depressão do segmento ST — que são invisíveis em repouso. has limited sensitivity, detecting only a fraction of CMR-confirmed events[30]. CMR with LGE is the most sensitive exame não invasivoA non-invasive test is a diagnostic procedure that obtains information about the body without breaking the skin or entering a body cavity; the coronary artery calcium scan is described as non-invasive because it requires only a brief CT scan rather than catheterization or surgery. and is the reference standard for non-acute scar detection[30][36]. Echocardiographic regional wall-motion abnormalities and elevated high-sensitivity troponinaTroponin is a protein that leaks into the blood when heart muscle is damaged. A blood test for it is how heart attacks are confirmed. in non-acute contexts may also raise suspicion.

7.7 Master-athlete-specific burden: the “masked athlete” phenomenon

In a seminal cross-sectional studyA cross-sectional study takes a single snapshot of a population at one moment., Katzel and colleagues found that approximately 16% of male master athletes (mean age 60 years) had silent ischemia on a symptom-limited graded exercise test, a prevalence statistically comparable to that observed in sedentary controls of similar age[23]. Athletic status did not reduce the prevalence of ischemic burden; rather, it changed the perception of that burden. Combined with the EIH literature[25][26], these findings support the concept of the masked athlete — an individual whose high cardiorespiratory fitness and elevated pain thresholds can defer the perception of ischemia until exertional demand approaches the limits of coronary supply.

CMR-LGE prevalence in master endurance athletes has been variably reported, ranging from approximately 11% in younger marathon runners to considerably higher figures in older endurance-athlete cohorts[37][38]. Ischemic-pattern LGE (subendocardial enhancement in a coronary distribution) and non-ischemic LGE (focal patchy enhancement at the right-ventricular hinge points or mid-myocardium) carry different mechanistic implications and different prognostic weights[36]. A sudden or unexplained decline in performance or in V̇O₂max in a previously stable master athlete should therefore be treated as a clinical red flag warranting consideration of advanced imaging.

8. Coronary Microvascular Dysfunction

Coronary microvascular dysfunction (CMD) is a plausible contributor to exercise intolerance in some older athletes, but the relevant evidence base in master-athlete cohorts is limited and findings should be described cautiously[39][40]. In a selected cohort of athletes with abnormal exercise tests but no obstructive epicardial CAD on angiotomografia coronarianaA angiografia coronária por tomografia computadorizada, ou CCTA, é um exame de tomografia computadorizada realizado com a injeção de um contraste nas veias, que produz imagens detalhadas das artérias do coração., Foulkes and colleagues reported significantly lower coronary flow reserveCoronary flow reserve compares blood flow through the heart's arteries at rest with flow when the heart is working hard. (3.3 vs 4.2 in controls) and elevated endothelin-1 levels[39]. Several mechanisms have been proposed in athletes specifically, including the hypothesis of a possible “capillary-to-myocyte mismatch” in which training-induced hypertrophy outpaces microvascular expansion. These findings are best interpreted as preliminary and hypothesis-generating rather than as evidence that CMD broadly explains performance decline across the master-athlete population.

CMD may present with atypical features, including reduced exercise capacityExercise capacity is a quantitative measure of the maximum physical work a person can perform, typically assessed during a graded stress test as peak workload in watts, peak oxygen consumption (VO2 max), or metabolic equivalents (METs). In the article, a decline in exercise capacity four months after stenting indicated that the procedure alone had not resolved the underlying disease., unusually elevated heart rates during submaximal effort, and exertional dyspnea rather than classic chest pain[40]. Diagnosis typically requires specialized testing (PET-based coronary flow reserve, invasive coronary physiology with bolus thermodilution, or stress CMR) available at experienced centers.

9. Screening and Risk Stratification in the Master Athlete

Given the high prevalence of subclinical CAD and silent ischemia in older athletes, traditional screening tools have important limitations. The resting 12-lead ECG, while valuable for detecting electrical disorders, has low sensitivity for aterosclerose subclínicaAterosclerose subclínica significa que há presença de placa, mas ela ainda não causou nenhum sintoma ou evento.[45]. Exercise treadmill testingA standardized clinical test in which a patient walks or runs on a treadmill at progressively increasing speeds and inclines while heart rate, blood pressure, and ECG are monitored; it can estimate cardiorespiratory fitness and detect myocardial ischemia. in asymptomatic athletes is constrained by high false-positive rates[44]. Importantly, individual tests should be selected according to the clinical question being asked — anatomy, inducible ischemia, prior scar, or microvascular function — rather than by pooled performance metrics across these distinct domains.

Tabela 4. Cardiac diagnostic modalities in older master athletes, organized by the clinical question each test answers.

Modalidade	Primary question answered	Main strength	Main limitation
Resting 12-lead ECG	Electrical disease; prior Q-wave MI	Widely available baseline test	Low sensitivity for silent CAD or non-Q-wave prior MI
Exercise treadmill ECG	Exercise-provoked ECG abnormalities; symptom correlation	Functional provocation; reveals exercise BP response	Both false positives and false negatives are common in master athletes: the latter because high cardiorespiratory reserve and collateral flow may allow some athletes to maintain workload despite inducible ischemia until higher exercise intensities
Coronary CT angiography (CCTA)	Coronary anatomy; plaque burden and stenosis	Strong anatomic definition of plaque/stenosis	Does not directly establish inducible ischemia
Stress echocardiography / stress perfusion imaging (SPECT, PET, stress CMR)	Inducible ischemia	Functional assessment of ischemic burden	Performance depends on protocol and image quality
CMR with LGE	Prior infarction / scar / fibrosis pattern (UMI)	High tissue characterization value; gold standard for non-acute scar	Not a primary test for obstructive CAD
PET with coronary flow reserve	Inducible ischemia plus microvascular function	Useful for CMD assessment in specialized centers	Limited availability; higher complexity

Sources: refs [40][44][45]. CCTA = coronary CT angiography; CMR = cardiac magnetic resonance; LGE = late gadolinium enhancement; UMI = unrecognized myocardial infarction; CMD = coronary microvascular dysfunction; SPECT = single-photon emission tomografia computadorizadaComputed tomography, or CT, takes X-ray images from many angles and reconstructs them into cross-sections of the body.; PET = positron emission tomography. The table is intentionally structured by clinical question rather than by pooled sensitivity/specificity, because tests answering different reference-standard questions are not directly comparable.

O Estudo ISCHEMIAThe International Study of Comparative Health Effectiveness with Medical and Invasive Approaches randomized 5,179 patients with stable coronary artery disease and moderate-to-severe ischemia to an upfront invasive strategy or medical therapy alone, finding no significant difference in the primary composite cardiovascular endpoint. should not be summarized as proving that exercise capacity outweighs coronary anatomy or ischemia severity. A more defensible conclusion from the ISCHEMIA program is that, in stable chronic coronary disease, an initial invasive strategy did not produce an overall reduction in major cardiovascular events compared with an initial conservative strategy, and prognosis varied according to disease burden in pre-specified analyses[41][42]. The broader point that cardiorespiratory fitness is a strong predictor of mortality is robustly supported by cardiopulmonary exercise testing literature outside the ISCHEMIA program[43]. For master athletes, the practical implication is that a sudden or unexplained decline in performance or in V̇O₂max should be treated as a clinical signal warranting structured evaluation[47].

10. Sex Differences and the Female Master Athlete

A substantial portion of the master-athlete coronary literature is derived from male cohorts, including Master@Heart, which enrolled only men[15]. In female master athletes, CAC prevalence is generally lower than in male counterparts at the same age and training exposure, and the coronary phenotype associated with lifelong endurance training is less well characterized[48]. The 2020 ESC Sports Cardiology Guideline emphasizes individualized risk assessment in female master athletes, with attention to traditional risk factors, menopausal status, and exercise pressão arterialA pressão arterial é a força do sangue empurrando as paredes das artérias. Ela é escrita como dois números, como 120/80. O número superior é a pressão quando o coração se contrai, o inferior é quando ele relaxa. response[47]. Generalizing male-cohort findings to female master athletes is inappropriate until parallel data are available.

11. Clinical Principles for the Aging Master Athlete

Current evidence supports individualized training and cardiovascular risk management rather than a single proven training formula for preventing coronary plaque in master athletes. Practical principles supported by primary literature and major-society guidance include:

• Maintain regular endurance activity at intensities and volumes appropriate to the individual, recognizing that detraining accelerates V̇O₂max decline beyond what biological aging alone produces[2][3].
• Incorporate treinamento de resistênciaO treinamento de resistência é o trabalho dos músculos contra uma carga — pesos, elásticos ou o peso do seu próprio corpo. to help preserve muscle mass and function across the aging trajectory.
• Aggressively manage conventional cardiovascular risk factors — LDL-cholesterol or apolipoprotein B, lipoprotein(a) where available, blood pressure, glycemia, and tobacco exposure — in accordance with current prevention guidelines[45][49][50].
• Evaluate exaggerated exercise blood pressure responses, which are independently associated with higher coronary plaque burden in master athletes[18].
• Treat unexplained performance decline as a clinical signal warranting structured assessment, given the “masked athlete” phenomenon[23][25].
• Apply advanced imaging (CCTA, stress imaging, CMR with LGE) selectively, guided by clinical context, exercise findings, and conventional risk profile[47].

Polarized training distributions (commonly described as approximately 80/20 low- to high-intensity) may be useful performance optimization frameworks but have não been prospectively shown to prevent CAC accrual or to mitigate the so-called paradoxo do atletaThe athlete paradox is the observation that some lifelong endurance athletes have higher coronary artery calcium scores and greater total plaque burden than less active peers, despite otherwise favorable cardiovascular risk profiles, suggesting that extreme chronic exercise may independently promote arterial calcification., and should not be presented as preventive prescriptions[51][52].

12. Synthesis and Discussion

12.1 Inevitable versus modifiable decay

The SPAF study confirms that the rise and fall of physical capacity is a constitutive feature of human life[1]. The age of peak performance and the acceleration of decline after age 40 appear largely invariant across populations. However, master athletes demonstrate that the absolute level of performance and the decadal rate of V̇O₂max loss are highly modifiable through maintenance of training volume and intensity[2][3][4].

12.2 Dominance of central factors

Between ages 50 and 80, the primary driver of performance decline in master athletes is central: a relentless decline in HR_max reduces total cardiac output during peak exertion, a limitation that even aggressive training cannot reverse[7]. Although athletes preserve stroke volume better than sedentary peers, age-related myocardial stiffening eventually restricts diastolic filling at high heart rates[10][11].

12.3 The pathological paradox

Lifelong endurance training appears associated with both favorable cardiovascular adaptation and an increased prevalence of subclinical coronary atherosclerosis in some observational cohorts[15][16][17]. The atherosclerotic burden — combined with the analgesic effects of exercise-induced hypoalgesia — makes silent ischemia and unrecognized MI clinically important risks that warrant individualized screening and management[23][25][26].

12.4 Peripheral mechanisms at the limit of human aging

As athletes approach age 80, peripheral extraction increasingly catches up to central factors as a determinant of V̇O₂max. Capillary rarefaction and mitochondrial decay reduce the muscle’s capacity to utilize delivered oxygen — an effect that is accelerated when training volume is reduced[2][9].

Key Clinical Takeaways

• Aerobic capacity declines along a curvilinear trajectory beginning in the mid-30s and accelerating in the 60s. Master athletes who maintain training reduce the rate of decline to roughly half that of sedentary peers; detraining accelerates decline several-fold. • Lifelong endurance training does not confer immunity to coronary atherosclerosis. Master@Heart and related cohorts show higher coronary calcium and proximal plaque burden in lifelong athletes than in sedentary peers; plaque morphology may be more favorable but does not abolish risk. • Silent ischemia and unrecognized myocardial infarction are not uncommon in older athletes. Approximately 1 in 6 male master athletes has inducible ischemia on graded exercise testing; CMR-detected scar in community cohorts exceeds ECG-detected scar by more than 2:1. • Symptoms may be absent, atypical, or expressed as performance loss. An unexplained decline in race times, exertional dyspnea, or reduced exercise tolerance in an older athlete should prompt structured cardiac evaluation — not reassurance. • Choose the diagnostic test to match the clinical question. Anatomy (CCTA), inducible ischemia (stress imaging), prior scar (CMR with LGE), and microvascular function (PET with CFR) answer different questions and are not interchangeable. • Standard cardiovascular risk-factor management remains the foundation. Aggressively manage LDL-C/ApoBApoB é uma proteína presente na parte externa de cada partícula de colesterol que pode ficar presa na parede da sua artéria e causar placa. Cada uma dessas partículas carrega exatamente uma ApoB., lipoprotein(a) where available, blood pressure (including exaggerated exercise responses), glycemia, and tobacco exposure. No training distribution has been prospectively shown to prevent CAC accrual. • Overall health benefits of lifelong exercise remain substantial. The clinical task is calibration of intensity, surveillance, and risk-factor control — not avoidance of training.

13. Conclusions

For master athletes between the ages of 50 and 80, maintenance of endurance performance requires a careful balance between sustained training (to preserve V̇O₂max and skeletal-muscle oxidative capacity) and individualized cardiovascular risk management. Transitioning from active to sedentary status produces a V̇O₂max decline substantially steeper than aging alone[2][3].

However, the masked athlete concept warrants vigilance rather than complacency. Older endurance athletes may present with reduced performance capacity, exertional dyspnea, or other atypical symptoms rather than classic angina, and unexplained decline in performance should prompt structured clinical reassessment[23][25][47].

The available literature supports substantial overall health benefits of long-term exercise[43][53]. Some evidence suggests that the fenótipo da placaPlaque phenotype refers to the biological and structural characteristics of an atherosclerotic lesion — including the size of its lipid-rich necrotic core, fibrous cap thickness, degree of calcification, and inflammatory cell content — which together determine whether a plaque is stable or at high risk of rupturing. of lifelong athletes is shifted toward more calcified and fewer mixed/non-calcified lesions when matched for total plaque burden, which may confer relative stability compared with sedentary patients of equivalent CAC score[16]. Even granting that observation, however, the present evidence base does not justify claiming that coronary calcificaçãoCalcification is when calcium gets deposited into a plaque, turning part of it hard and bony. in master athletes is uniformly benign, or that mortality advantages persist regardless of plaque phenotype — CAC-stratified mortality data specific to master athletes remain limited. A more evidence-consistent conclusion is that lifelong exercise and subclinical coronary disease can coexist, that plaque morphology likely matters as well as plaque quantity, and that individualized risk assessment is essential in older athletes.

14. Limitations

This is a narrative review. No systematic search protocol or formal meta-analytic pooling was performed. The Master@Heart cohort and several other key coronary-imaging studies in lifelong endurance athletes are all-male, limiting generalizability to female master athletes. CAC-stratified mortality data specific to master athletes remain sparse, and the prognostic significance of non-calcified proximal plaques identified incidentally on CCTA in asymptomatic athletes is not yet established. The relevant CMD literature in master athletes is derived from small selected cohorts on referral and should not be generalized.

Disclosures and End-Matter

Conflicts of interest

The author reports no financial conflicts of interest related to the subject matter of this manuscript. The author is the operator of CuringHeartDisease.com, a clinician-educator platform that provides peer-reviewed cardiovascular health content without supplement marketing or commercial sponsorship.

Funding

No external funding, sponsorship, or institutional support contributed to the conception, drafting, or publication of this manuscript.

Data availability

No new datasets were generated for this narrative review. All cited evidence is contained in the published literature and is accessible through the cited references.

Ethics

Ethics approval and informed consent were not required because this manuscript is a review of previously published literature and does not report new human-subject research.

Prior dissemination

No version of this manuscript has been previously published or made publicly available in any venue, including preprint servers and the author’s educational platform. CuringHeartDisease.com is the intended publication venue.

Author contributions

PM conceived the manuscript, conducted the literature identification, drafted and revised the text, and approved the final version for publication.

Acknowledgments

The author thanks the external reviewers whose comments informed the present revision.

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